Juvenile Periodontitis Research Articles

Flp-1, the first representative of a new pilin gene subfamily, is required for non-specific adherence of Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans, a Gram-negative bacterium responsible for localized juvenile periodontitis and other infections such as endocarditis, produces long fibrils of bundled pili that are believed to mediate non-specific, tenacious adherence to surfaces. Previous investigations have implicated an abundant, small ( approximately 6.5 kDa), fibril-associated protein (Flp/Fap) as the primary fibril subunit. Here, we report studies on fibril structure and on the function and evolution of Flp. High-resolution electron microscopy of adherent clinical strain CU1000N revealed long bundles of 5- to 7-nm-diameter pili, whose subunits appear to be arranged in a helical array similar to that observed for type IV pili in other bacteria. Fibrils were found to be associated with the bacterial cell surface and smaller structures thought to be membrane vesicles. A modified version of the CU1000N Flp1 polypeptide with the T7-TAG epitope fused to its C-terminus was expressed in the wild-type strain, and the presence of the modified Flp1 in fibrils was confirmed by immunogold electron microscopy with monoclonal antibody to T7-TAG. To determine the importance of Flp1 in fibril formation and cell adherence, we used transposon IS903phikan to isolate insertion mutations in the flp-1 gene (formerly designated flp). Mutants with insertions early in flp-1 fail to produce fibrils and do not adhere to surfaces. Both fibril production and adherence were restored by cloned flp-1 in trans, thus providing the first evidence that flp-1 is required for fibril formation and tight, non-specific adherence. One mutant was found to have an insertion near the 3' end of flp-1 that results in the expression of a truncated and altered C-terminus of Flp1. This mutant produced short, unbundled pili, and its adherence to surfaces was significantly less than that of wild-type bacteria. These findings and related observations with the Flp1-T7-TAG protein indicate that the C-terminus of Flp1 is important for the bundling and adherence properties of pili. Extensive sequence comparisons and phylogenetic analysis of 61 predicted prepilin genes of bacteria revealed flp-1 to be a member of a novel and widespread subfamily of type IV prepilin genes. Thus, Flp pili are likely to be expressed by diverse bacterial species. Furthermore, we found that it is common for bacterial genomes to contain multiple alleles of flp-like genes, including the open reading frame (flp-2, previously designated orfA) immediately downstream of flp-1 in A. actinomycetemcomitans. The duplication and divergence of flp genes in bacteria may be important to the diversification of the colonization properties of these organisms.

External resorption associated with tooth eruption

A case is presented with severe resorption on the mesial root of the mandibular first permanent molar in a patient with Juvenile Periodontitis. The follicle of the bicuspid is seen in contact with mesial root of the molar.

Microbiological characteristics of subgingival microbiota in adult periodontitis, localized juvenile periodontitis and rapidly progressive periodontitis subjects

To describe the prevalence of the cultivable subgingival microbiota in periodontal diseases and to draw attention to the polymicrobial nature of periodontic infections. The study population consisted of 95 patients, 51 females and 44 males, aged 14-62 years. Twenty-nine patients exhibited adult periodontitis (AP), six localized juvenile periodontitis (LJP), and 60 rapidly progressive periodontitis (RPP). Two to four pooled bacterial samples were obtained from each patient. Samples were collected with sterile paper points from the deepest periodontal pockets. The samples were cultured under anaerobic and microaerophilic conditions using selective and non-selective media. Isolates were characterized to species level by conventional biochemical tests and by a commercial rapid test system. Prevotella intermedia and Capnocytophaga spp. were the most frequently detected microorganisms in all diagnostic groups. Porphyromonas gingivalis and Peptostreptococcus micros were found more frequently in AP and RPP patients, while Actinobacillus actinomycetemcomitans and Eikenella corrodens were associated with AP, LJP and RPP patients. The other bacterial species, including Actinomyces spp., Streptococcus spp. and Eubacterium spp., were detected at different levels in the three disease groups. The data show the complexity of the subgingival microbiota associated with different periodontal disease groups, indicating that the detection frequency and levels of recovery of some periodontal pathogens are different in teeth affected by different forms of periodontal disease.

Detection rate of Actinobacillus actinomycetemcomitans on the permanent 1st molars of primary school children in Taiwan by polymerase chain reaction.

Actinobacillus actinomycetemcomitans (Aa) has been implicated as the putative micro-organism for localized juvenile periodontitis (LJP). The most distinct clinical features of LJP include severe angular bony defects of the mesial sides of permanent first molars and the onset of disease during puberty. Currently, no large-scale studies have been performed which address the change in detection rates of Aa on the mesial sides of permanent 1st molars following eruption and up to puberty. In this study, subgingival plaque samples were taken from the mesial pockets of 2 randomly selected permanent 1st molars from 328 primary school children and 50 adult staff, and analyzed by polymerase chain reaction (PCR) to detect Aa. The results showed a 5.5% prevalence rate of Aa which increased after the eruption of 1st molars and peaked near puberty. There were no significant differences in the detection rates of Aa among different groups in terms of gender, plaque index (PII), and gingival index (GI); however, the higher detection rates of Aa were significantly associated with increased probing depths at p<0.05. PCR analysis of the subgingival plaques demonstrated a prevalence of Aa which peaked near puberty, suggesting that Aa may be important for LJP in Taiwan.

Anticorpos antileucotoxina contra Actinobacillus actinomycetemcomitans em amostras de soro e saliva de pacientes com periodontite juvenil localizada

The leukotoxin produced by Actinobacillus actinomycetemcomitans is considered the major virulence factor with potential to cause damage to the host defenses. The present work analyzed the serumal and salivary levels of antibodies against the leukotoxin produced by A. Actinomycetemcomitans, in patients with Localized Juvenile Periodontitis (LJP) and in healthy controls. Additionally, analysis of the immune complex (IC) was carried out in saliva samples. The classic ELISA method, with leukotoxin obtained through Sephadex G-200 gel filtration, and the capture ELISA method, using rabbit anti-A. Actinomycetemcomitans (leukotoxic, FDC Y4, IgG) adsorbed with a non-leukotoxic strain of A. actinomycetemcomitans, were used. The results obtained demonstrated significantly higher serumal levels of IgG in patients with LJP, when they were compared with the healthy controls, both for the classic and capture ELISA methods (p < 0.05). However, no significant differences were observed between the salivary levels of IgG, SIgA and IC in the examined individuals. These results suggest that even though A. actinomycetemcomitans presents virulence factors that affect the immune response, there is immune response to leukotoxin in LJP patients. This increase of IgG in the blood stream might contribute to host defense, limiting the lesion to the periodontal regions already colonized by A. actinomycetemcomitans.

Beyond the specific plaque hypothesis: are highly leukotoxic strains of Actinobacillus actinomycetemcomitans a paradigm for periodontal pathogenesis?

Actinobacillus actinomycetemcomitans is a facultative anaerobe implicated in a variety of periodontal diseases. Its presence is most closely associated with localized juvenile periodontitis (LIP), although the exact role of the organism in this and other periodontal diseases is not entirely clear. While A. actinomycetemcomitans produces several different putative virulence factors, the most widely studied is the leukotoxin. The leukotoxin selectively kills polymorphonuclear leukocytes and macrophages in vitro, constituting the host's first line of defense. Interestingly, even though all strains of A. actinomycetemcomitans have the genes encoding the leukotoxin, there is variability in leukotoxin expression. Differences in the structure of the promoter region of the leukotoxin gene operon were shown to correlate directly with levels of leukotoxin production. Highly leukotoxic forms appear to exhibit increased pathogenic potential, as evidenced by recent studies that have shown a significant association between the prevalence of such strains and the occurrence of LIP in several different populations. This represents the first demonstration of an association between a particular subset of a pathogenic species and a specific periodontal disease. Early identification of A. actinomycetemcomitans by microbial and genetic assays to evaluate leukotoxicity may enhance the efficacy of preventive and/or therapeutic techniques. Future investigations should continue to evaluate pathogenic variations of additional virulence factors expressed in vivo, not only of A. actinomycetemcomitans, but also of other periodontal bacteria and infectious disease pathogens.

Improved, Low-Cost Selective Culture Medium for Actinobacillus actinomycetemcomitans

Actinobacillus actinomycetemcomitans is considered to be one of the major oral putative pathogens, especially in cases of juvenile periodontitis. This microorganism requires nutritionally complex media for growth, and therefore the media for its primary isolation usually include blood agar or serum in their base. In this study we present a new medium, Dentaid-1, which improves the detection of A. actinomycetemcomitans in periodontal samples. In its composition, blood and serum have been omitted, hence reducing its cost and making it a more restrictive medium against the growth of other microorganisms with high nutritional requirements. The growth yields of pure cultures of the bacteria on Dentaid-1 were comparable to those on nonselective blood agar. Moreover, clinical efficacy was evaluated in subgingival samples from 77 subjects with adult periodontitis. Dentaid-1 detected A. actinomycetemcomitans in 24 subjects, while a previously described tryptic soy-serum-bacitracin-vancomycin agar detected the microorganism in only 19 subjects (79.1%). Dentaid-1 is a low-cost, noninhibitory formula for the improved diagnosis and monitoring of patients subgingivally infected by this important oral putative pathogen.

Nonsurgical periodontal therapy.

Regular home care by the patient in addition to professional removal of subgingival plaque is generally very effective in controlling most inflammatory periodontal diseases. When disease does recur, despite frequent recall, it can usually be attributed to lack of sufficient supragingival and subgingival plaque control or to other risk factors that influence host response, such as diabetes or smoking. Causative factors contributing to recurrent disease include deep inaccessible pockets, overhangs, poor crown margins and plaque-retentive calculus. In most cases, simply performing a thorough periodontal debridement under local anesthesia will stop disease progression and result in improvement in the clinical signs and symptoms of active disease. If however, clinical signs of disease activity persist following thorough mechanical therapy, such as increased pocket depths, loss of attachment and bleeding on probing, other pharmacotherapeutic therapies should be considered. Augmenting scaling and root planing or maintenance visits with adjunctive chemotherapeutic agents for controlling plaque and gingivitis could be as simple as placing the patient on an antimicrobial mouthrinse and/or toothpaste with agents such as fluorides, chlorhexidine or triclosan, to name a few. Since supragingival plaque reappears within hours or days after its removal, it is important that patients have access to effective alternative chemotherapeutic products that could help them achieve adequate supragingival plaque control. Recent studies, for example, have documented the positive effect of triclosan toothpaste on the long-term maintenance of both gingivitis and periodontitis patients. Daily irrigation with a powered irrigation device, with or without an antimicrobial agent, is also useful for decreasing the inflammation associated with gingivitis and periodontitis. Clinically significant changes in probing depths and attachment levels are not usually expected with irrigation alone. Recent reports, however, would indicate that, when daily irrigation with water was added to a regular oral hygiene home regimen, a significant reduction in probing depth, bleeding on probing and Gingival Index was observed. A significant reduction in cytokine levels (interleukin-1beta and prostaglandin E2, which are associated with destructive changes in inflamed tissues and bone resorption also occurs. If patient-applied antimicrobial therapy is insufficient in preventing, arresting, or reversing the disease progression, then professionally applied antimicrobial agents should be considered including sustained local drug delivery products. Other, more broadly based pharmacotherapeutic agents may be indicated for multiple failing sites. Such agents would include systemic antibiotics or host modulating drugs used in conjunction with periodontal debridement. More aggressive types of juvenile periodontitis or severe rapidly advancing adult periodontitis usually require a combination of surgical intervention in conjunction with systemic antibiotics and generally are not controlled with nonsurgical anti-infective therapy alone. It should be noted, however, that, to date, no home care products or devices currently available can completely control or eliminate the pathogenic plaques associated with periodontal diseases for extended periods of time. Daily home care and frequent recall are still paramount for long-term success. Nonsurgical therapy remains the cornerstone of periodontal treatment. Attention to detail, patient compliance and proper selection of adjunctive antimicrobial agents for sustained plaque control are important elements in achieving successful long-term results. Frequent re-evaluation and careful monitoring allows the practitioner the opportunity to intervene early in the disease state, to reverse or arrest the progression of periodontal disease with meticulous nonsurgical anti-infective therapy.

歯周組織の破壊と再生におけるサイトカインの役割について

Inflammatory bone resorption is a feature of chronic inflammatory diseases such as periodontitis and rheumatoid arthritis. In human periodontitis, certain species of Gramnegative bacteria harbored in periodontal pockets play a major part in the pathogenesis of the disease. Among these periodontopathic bacteria, Actinobacillus actinomycetemcomitans has been implicated as an etiological agent in juvenile and adult periodontitis. Localized juvenile periodontitis is characterized by alveolar bone loss mainly affecting the permanent first molars and incisors. It is known that bone resorption is associated with the generation and activation of osteoclasts, unique bone resorbing multinucleated cells. Osteoclasts are derived from the hematopoietic progenitors, and cytokines such as interleukin-1 (IL-1) and prostaglandins (PGs) can modulate osteoclastogenesis. In this regard, we have previously shown that lipopolysaccharide (LPS) and capsular polysaccharide from A. actinomycetemcomitans are likely to play mediative roles in the induction of alveolar bone-loss in periodontal diseases.Bone morphogenetic protein-2 (BMP-2) is a member of the transforming growth factor beta superfamily. While BMP-2 is capable of inducing bone formation ectopically, little is known about its role on osteoclastogenesis. We examined the effect of BMP-2 on osteoclast-like multinucleated cell (OCL) formation in cocultures of osteoblast-like cells and hematopoietic cells of bone marrow origin. BMP-2 strongly enhanced OCL formation in a dose-dependent fashion in the presence of IL-1α. Our findings indicated that BMP-2 may enhance bone resorption instead of bone formation in inflammatory environments, suggesting that the control of inflammatory reaction in the target tissues may be one of the critical steps in clinical application of BMPs.

Cloning and characterization of a gene encoding an immunosuppressive factor from Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans is a pathogen of localized juvenile periodontitis and adult periodontitis. Immunomodulating activity is generally thought to be important in colonization by such pathogenic bacteria. Among the proteins possessing these activities, a 14 kDa immunosuppressive factor of A. actinomycetemcomitans has been reported by Kurita-Ochiai and Ochiai (Infect Immun 64: 50-54, 1996). To evaluate this factor, we cloned and characterized the gene encoding it. The immunosuppressive factor was screened from a genomic library of A. actinomycetemcomitans using an oligonucleotide probe based on the amino acid sequence of the factor. The clone obtained, pHI13, contained a 1.5 kbp fragment. The immunosuppressive factor located in its center. Southern blot analysis showed that this factor is common among A. actinomycetemcomitans strains. The open reading frame consisted of 324 bp coding for 107 amino acid residues. The relative molecular mass of the deduced amino acid sequence was calculated to be 11,595. BLAST analysis indicated that the amino acid sequence is highly homologous with those of thioredoxins from Haemophilus influenzae (76.6%), Neisseria meningitidis (67.3%), and Pseudomonas aeruginosa (59.3%). These results suggest that the 14 kDa immunosuppressive factor characterized in this study is a thioredoxin.

The effect of flap operation and metronidazole gel combined therapy on the treatment of the juvenile periodontitis

The effect of flap operation and metronidazole gel combined therapy on the treatment of the juvenile periodontitis

The in vivo expression of the collagenolytic matrix metalloproteinases (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in adult and localized juvenile periodontitis.

Periodontal inflammation is characterized by irreversible degradation of periodontal ligament collagen fibers leading to loss of tooth attachment. Cultured gingival keratinocytes and fibroblasts express, in vitro, various matrix metalloproteinases (MMPs) which can degrade fibrillar collagens. We hypothesized that several MMPs are also synthesized in vivo by sulcular epithelium, and analyzed the collagenolytic MMPs (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in gingival tissue specimens and gingival crevicular fluid from adult and localized juvenile periodontitis patients by in situ hybridization, immunohistochemistry, and Western immunoblotting. MMP-2, -7, -8, and -13 were expressed in gingival sulcular epithelium. MMP-7 and -13 were also located in fibroblasts and macrophages, and MMP-8 in neutrophils. MMP-8- and -13-positive cells/mm2 were higher in periodontitis gingiva when compared with healthy control tissue (p < 0.01). In periodontal diseases, gingival sulcular epithelium expresses several, rather than a single, collagenolytic MMPs, and this proteolytic cascade is evidently responsible for the tissue destruction characteristic of adult and juvenile periodontitis.

Long-term follow-up of successful orthodontic-periodontal treatment of localized aggressive periodontitis: a case report.

This report describes a case of localized aggressive periodontitis (localized juvenile periodontitis) that was jointly treated with conventional periodontal therapy, selective extractions to eliminate localized areas of vertical bone loss, and orthodontic therapy. A 20-year follow-up is described in this report. The success of periodontal treatment in a case such as this depends on making an accurate diagnosis, providing periodontal treatment to control the disease, and providing regular periodontal maintenance during and after orthodontic treatment.

Secretion of RTX leukotoxin by Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans, the etiologic agent for localized juvenile periodontitis and certain other human infections, such as endocarditis, expresses a leukotoxin that acts on polymorphonuclear leukocytes and macrophages. Leukotoxin is a member of the highly conserved repeat toxin (RTX) family of bacterial toxins expressed by a variety of pathogenic bacteria. While the RTX toxins of other bacterial species are secreted, the leukotoxin of A. actinomycetemcomitans is thought to remain associated with the bacterial cell. We have examined leukotoxin production and localization in rough (adherent) and smooth (nonadherent) strains of A. actinomycetemcomitans. We found that leukotoxin expressed by the rough, adherent, clinical isolate CU1000N is indeed cell associated, as expected. However, we were surprised to find that smooth, nonadherent strains of A. actinomycetemcomitans, including Y4, JP2 (a strain expressing a high level of toxin), and CU1060N (an isogenic smooth variant of CU1000N), secrete an abundance of leukotoxin into the culture supernatants during early stages of growth. After longer times of incubation, leukotoxin disappears from the supernatants, and its loss is accompanied by the appearance of a number of low-molecular-weight polypeptides. The secreted leukotoxin is active, as evidenced by its ability to kill HL-60 cells in vitro. We found that the growth phase and initial pH of the growth medium significantly affect the abundance of secreted leukotoxin, and we have developed a rapid (<2 h) method to partially purify large amounts of leukotoxin. Remarkably, mutations in the tad genes, which are required for tight nonspecific adherence of A. actinomycetemcomitans to surfaces, cause leukotoxin to be released from the bacterial cell. These studies show that A. actinomycetemcomitans has the potential to secrete abundant leukotoxin. It is therefore appropriate to consider a possible role for leukotoxin secretion in the pathogenesis of A. actinomycetemcomitans.

Herpesviruses: a unifying causative factor in periodontitis?

Human cytomegalovirus and Epstein-Barr virus type 1 are discussed in this review as they relate to destructive periodontal disease in humans. Genomes of the two herpesviruses occur frequently in severe adult periodontitis, localized and generalized juvenile periodontitis, Papillon-Lefèvre syndrome periodontitis, Down's syndrome periodontitis, HIV-associated periodontitis and acute necrotizing ulcerative gingivitis. Herpesvirus infections generally involve a mild or asymptomatic primary phase followed by an asymptomatic latent phase interrupted sporadically by periods of activation, where viral replication and possibly clinical disease become manifest. Herpesvirus reactivation is triggered by a number of immunosuppressing factors, some of which have also been shown to be risk indicators of periodontal disease. Available evidence argues for the involvement of active cytomegalovirus infection in the initiation and progression of localized juvenile periodontitis and possibly other types of periodontal disease. In periodontal disease, herpesviruses may cause release of tissue-destructive cytokines, overgrowth of pathogenic periodontal bacteria, and initiation of cytotoxic or immunopathogenic events. Understanding the significance of herpesviruses in the causation and pathogenesis of destructive periodontal diseases may have important implications in future prevention and treatment of the diseases.

Clindamycin promotes phagocytosis and intracellular killing of periodontopathogenic bacteria by crevicular granulocytes: an in vitro study.

Phagocytosis of periodontopathogenic bacteria by crevicular polymorphonuclear neutrophil granulocytes (PMNs) plays a key role in the aetiology of periodontitis. Antimicrobials such as clindamycin have been proven to be effective in treating progressive forms of this disease. Therefore, the purpose of this study was to determine the effect of clindamycin on the phagocytosing properties of gingival crevicular PMNs obtained from 16 patients with rapidly progressive periodontitis (RPP), eight with localized juvenile periodontitis (LJP), 12 with adult periodontitis (AP) and 13 periodontally healthy controls. The phagocytosis assay was performed with the two strains Porphyromonas gingivalis ATCC 33277 and Actinobacillus actinomycetemcomitans Tanner FDC 44 on a slide. Phagocytosis and intracellular killing were assessed by fluorescence microscopy after staining with acridine orange. The addition of clindamycin elevated the percentage of phagocytosing PMNs in periodontitis patients and controls regardless of whether P. gingivalis or A. actinomycetemcomitans was used as test strain. In granulocytes of healthy controls an enhancement of the intracellular killing of both strains was observed if clindamycin was added. Besides the antimicrobial effect, the enhancement of the phagocytosis might be an additional indication for treatment of periodontitis patients with clindamycin.

Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis.

Actinobacillus actinomycetemcomitans leukotoxin is thought to be an important virulence factor in the pathogenesis of localized juvenile and other forms of early-onset periodontitis. Some highly leukotoxic A. actinomycetemcomitans strains produce 10 to 20 times more leukotoxin than other minimally leukotoxic strains. The distribution, clonality, and intrafamilial transmission of highly leukotoxic A. actinomycetemcomitans were examined in order to determine the importance of leukotoxin in the pathogenesis of periodontitis. The polymerase chain reaction (PCR) was used to differentiate highly leukotoxic from minimally leukotoxic strains in examining 1,023 fresh A. actinomycetemcomitans isolates and strains from our culture collection. These were obtained from 146 subjects including 71 with localized juvenile periodontitis (LJP), 4 with early-onset periodontitis, 11 with post-localized juvenile periodontitis, 41 with adult periodontitis, and 19 periodontally normal subjects. The arbitrarily primed polymerase chain reaction (AP-PCR) analysis of 30 oral isolates from each of 25 subjects was used to determine the intraoral distribution of A. actinomycetemcomitans clones. AP-PCR was also used to examine the transmission of A. actinomycetemcomitans in 30 members of 6 families. The clonality of 41 highly leukotoxic A. actinomycetemcomitans strains was evaluated by both AP-PCR and ribotyping. Highly leukotoxic A. actinomycetemcomitans was found only in subjects with localized juvenile and early-onset periodontitis. Fifty-five percent of the LJP subjects harbored highly leukotoxic A. actinomycetemcomitans isolates. Seventy-three percent of the A. actinomycetemcomitans isolates in these subjects were highly leukotoxic. Highly leukotoxic A. actinomycetemcomitans infected younger subjects (mean age 13.95 years, range 5 to 28 years) than minimally leukotoxic (mean age 35.47 years, range 6 to 65 years). Most subjects were infected with only one A. actinomycetemcomitans genotype. However, PCR of whole dental plaques and subsequent analysis of up to 130 individual oral isolates suggested a possible shift in A. actinomycetemcomitans over time in that a few subjects harbored both highly leukotoxic and minimally leukotoxic strains. AP-PCR analysis was consistent with intrafamilial A. actinomycetemcomitans transmission. Ribotyping and AP-PCR analysis confirmed a previous report that highly leukotoxic A. actinomycetemcomitans consists of a single clonal type. This study suggests that localized juvenile and other forms of Actinobacillus-associated periodontitis are primarily associated with the highly leukotoxic clone of A. actinomycetemcomitans.

Human herpesviruses and Porphyromonas gingivalis are associated with juvenile periodontitis.

Although herpesviruses have been associated with adult periodontitis, their relationship with juvenile periodontitis (JP) has not been established. This case-control study examined possible associations between JP and pathogenic bacteria, the human cytomegalovirus (HCMV), and the Epstein-Barr type 1 virus (EBV-1). Subjects were participants in a larger survey of schoolchildren in North-Central Jamaica. Subgingival plaque samples from 15 subjects with JP, 20 with incipient periodontitis (IP), and 65 randomly-selected healthy controls were assayed for Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans using a 16S rRNA polymerase chain reaction (PCR) identification method, and for HCMV and EBV-1 using nested PCR identification. Strong bivariate associations were found between JP and P. gingivalis (odds ratio [OR] = 12.7; 95% CI = 2.6, 61.4), HCMV (OR = 10.0; 95% CI = 2.7, 36.3), and A. actinomycetemcomitans (OR = 8.0; 95% CI = 2.3, 27.5), but not EBV-1. In multivariate analyses, P. gingivalis remained a significant explanatory variable (OR = 7.8; 95% CI = 1.5, 40.9); however, the associations were marginal for HCMV (OR = 4.6; 95% CI = 0.9, 22.7), and non-significant for A. actinomycetemcomitans (OR = 2.0; 95% CI = 0.4, 9.7). The associations with JP and the extent of attachment loss were even stronger when both P. gingivalis and HCMV were detected together. P. gingivalis (OR = 3.9; 95% CI = 1.3, 12.0) and EBV-1 (OR = 3.3; 95% CI = 1.0, 10.3) were the only significant explanatory variables in the multivariate analysis of IP. P. gingivalis is the strongest and most stable indicator of periodontitis in Jamaican adolescents. Co-infection with P. gingivalis and HCMV appears to be particularly deleterious to periodontal health.

Proximal caries in juvenile periodontitis patients.

Caries is recognized as the prevalent proximal dental disease in adolescents, while proximal bone loss is minimal to non-existent in this population. Adolescents demonstrating an inverse disease pattern, i.e., minimal caries and active periodontitis, could provide powerful clues with regard to both diseases. However, data are inconsistent. This study was designed to clarify this relationship by comparing proximal caries prevalence in a juvenile periodontitis (JP) group to a matched non-periodontally diseased control group. Two groups (cases [JPs] and control patients [CPs]) were matched for age, sex, and race and evaluated for decayed, missing, filled teeth and surfaces (DMFS) by radiographic analysis. Statistical analysis was performed by ANOVA and Student t test. The study consisted of four phases. Phase I was based on data from a previous study that failed to include race in the analysis. Thus, the original 23 JP patients (mostly African-Americans from New York City) were rematched for race as well as sex and age with CPs from Newark, NJ. The effect of water fluoridation (found in NYC) was evaluated in Phase II by matching the 23 original CPs (mostly Caucasian from NYC) with 23 CPs from NJ. Since differences were seen, we rematched our original JPs from NYC with a new set of race-matched CPs from NYC (Phase III). Finally, 13 JP patients from the University of Medicine and Dentistry of New Jersey (UMDNJ) were matched with CPs from NJ (Phase IV). Phase I and III indicated that JP patients had significantly less proximal caries than their matched CPs (P < or =0.05). Phase II confirmed the role of fluoride in caries reduction. Phase IV (NJ sample) supported our previous data and suggested that JP patients had less proximal caries than CPs (P < or =0.05). JP patients had significantly less proximal caries than their matched CPs when groups were balanced and radiographic evaluations were performed. In-depth studies of JP patients could provide important clues about both caries and periodontal disease etiology and pathogenesis.

Genetic polymorphisms of the IL-1alpha and IL-1beta genes in African-American LJP patients and an African-American control population.

A functional polymorphism of the interleukin-1 beta (IL-1beta) gene has been proposed to be a risk factor for periodontitis. In adult forms of periodontitis, non-smokers of northern European heritage carrying the "2" allele of the IL-1alpha-889 and the IL-1beta +3953 RFLPs in either the heterozygous or the homozygous state at both loci were observed to have a greater risk for developing severe periodontitis. Studies of early-onset periodontitis (EOP) found that allele "1" of both IL-1alpha-889 and IL-1beta +3953 was transmitted more frequently with the EOP phenotype. The purpose of the present study was to determine the prevalence of the IL-1alpha and IL-1beta genotype polymorphisms in an African-American (AA) control population and in 37 African-Americans with localized juvenile periodontitis (LJP). The IL-1alpha +4845 and IL-1beta +3953 loci were genotyped by PCR amplification, followed by restriction enzyme digestion and gel electrophoresis. The IL-1alpha +4845 locus, in linkage disequilibrium (>99%) with IL-1alpha-889, was genotyped because it is technically easier. Data were analyzed using r x c contingency tables. The IL-1beta +3953 allele "1" was carried by >99% of the AA control population and by 100% of the AA LJP group, with most individuals being homozygous 1,1. The prevalence of the composite genotype with at least one allele "2" at each of the IL-1beta +3953 and IL-1alpha +4845 loci was 14% (AA control group) and 8% (AA LJP group). Given the high frequency of the IL-1beta allele "1" in the African-American population, it would appear that knowledge of this +3953 polymorphism would provide little diagnostic or predictive information for LJP.